Also found in: Medical.
Related to thrombogenesis: fibrinolysis, Extrinsic pathway


n. trombogénesis, formación de cóagulos o trombos.
References in periodicals archive ?
Cardiovascular instability, such as increased myocardial work and increased risk of tachydysrhythmia, promotes thrombogenesis and platelet activation after ROSC and adverse immunomodulatory and metabolic effects.
Vascular Gas6 contributes to thrombogenesis and promotes tissue factor upregulation after vessel injury in mice.
pylori can cause increased thrombogenesis by increasing levels of lipids, triglyceride, TNF and IL-6 in the plasma; subsequently all of these will cause inflammation and promote clot formation at the site of a previous atherosclerotic lesion.
Exercise-induced changes in inflammatory processes: Implications for thrombogenesis in cardiovascular disease.
Differential effects of alpha- and gamma-tocopherol on low-density lipoprotein oxidation, superoxide activity, platelet aggregation and arterial thrombogenesis.
Increased von Willebrand factor in the endocardium asa local predisposing factor for thrombogenesis in overloaded human atrial appendage.
Available data suggest that low magnesium levels may promote endothelial cell dysfunction and greater tendency of thrombogenesis by increasing platelet aggregation and vascular calcifications14.
Repetitive trauma causes intimal damage and thrombogenesis.
D-dimer, the main breakdown fragment of fibrin, is a biochemical marker of thrombogenesis and fibrin turnover.
level may promote endothelial cell dysfunction and thrombogenesis by increasing platelet aggregation and vascular calcification.
2] receptor) significantly accelerated thrombogenesis, reflected by shortened time to vascular occlusion after photochemical injury of the carotid artery and reduced thrombogenesis after laser-induced cremaster arterioles injury [5]; however, these effects were not observed in either global or myeloid cell mPGES-1 knockout mice [10,13].
These incredible results concerning higher risk of mortality have led to doubt that widespread precursors predispose to diabetes and CHD with subsequent implications that insulin resistance, visceral adiposity, and excess inflammation cause the pathophysiology of thrombogenesis.